Immunological aspects of type 1 and 2 diabetes mellitus.
(1985) In Advances in Experimental Medicine and Biology 189. p.107-127- Abstract
IDDM occurs predominantly among individuals being class II antigen HLA-DR 3 and/or 4 positive, while NIDDM is not associated with HLA-D. Although the HLA-DR 3 or 4 specificities are prerequisites for IDDM to develop, their high frequencies (about 60%) in the background population preclude tissue typing as a predictive test, underlined by the observation that less than 50% of monozygotic twins are concordant for IDDM. The presence of a number of immune abnormalities argues that the causes of IDDM may be sought in an altered immune reaction against antigens present in the pancreatic B cells and/or in the environment. The majority of IDDM patients of short duration show both cellular and humoral autoimmunity against the pancreatic B cells.... (More)
IDDM occurs predominantly among individuals being class II antigen HLA-DR 3 and/or 4 positive, while NIDDM is not associated with HLA-D. Although the HLA-DR 3 or 4 specificities are prerequisites for IDDM to develop, their high frequencies (about 60%) in the background population preclude tissue typing as a predictive test, underlined by the observation that less than 50% of monozygotic twins are concordant for IDDM. The presence of a number of immune abnormalities argues that the causes of IDDM may be sought in an altered immune reaction against antigens present in the pancreatic B cells and/or in the environment. The majority of IDDM patients of short duration show both cellular and humoral autoimmunity against the pancreatic B cells. Similar phenomena may be observed in patients initially diagnosed as NIDDM and treated with oral hypoglycemic agents. It has been speculated that these patients have a retarded form of IDDM. It is possible that the combination of specific Class II antigen molecule(s) and an invading antigen (virus, bacterium, chemical etc.) presented to the immune system triggers the formation of effector cells such as B lymphocytes and cytotoxic T lymphocytes which also cross-react with the pancreatic B cells. Multiple exposures to this or related antigens throughout several years may eventually lead a sufficient loss of pancreatic B cells to cause insulin dependence.
(Less)
- author
- Lernmark, A. LU ; Baekkeskov, S. ; Gerling, I. ; Kastern, W. ; Knutson, C. and Michelsen, B.
- publishing date
- 1985-01-01
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- subject
- host publication
- Comparison of Type I and Type II Diabetes : Similarities and Dissimilarities in Etiology, Pathogenesis, and Complications - Similarities and Dissimilarities in Etiology, Pathogenesis, and Complications
- series title
- Advances in Experimental Medicine and Biology
- editor
- Vranic, Mladen ; Hollenberg, Charles H and Steiner, George
- volume
- 189
- pages
- 107 - 127
- external identifiers
-
- pmid:4036712
- scopus:0021783009
- ISSN
- 0065-2598
- ISBN
- 978-1-4757-1852-2
- 978-1-4757-1850-8
- DOI
- 10.1007/978-1-4757-1850-8_7
- language
- English
- LU publication?
- no
- id
- f5712ceb-f15c-483d-a345-de704240795c
- date added to LUP
- 2019-09-16 12:39:31
- date last changed
- 2024-03-13 08:23:08
@inbook{f5712ceb-f15c-483d-a345-de704240795c, abstract = {{<p>IDDM occurs predominantly among individuals being class II antigen HLA-DR 3 and/or 4 positive, while NIDDM is not associated with HLA-D. Although the HLA-DR 3 or 4 specificities are prerequisites for IDDM to develop, their high frequencies (about 60%) in the background population preclude tissue typing as a predictive test, underlined by the observation that less than 50% of monozygotic twins are concordant for IDDM. The presence of a number of immune abnormalities argues that the causes of IDDM may be sought in an altered immune reaction against antigens present in the pancreatic B cells and/or in the environment. The majority of IDDM patients of short duration show both cellular and humoral autoimmunity against the pancreatic B cells. Similar phenomena may be observed in patients initially diagnosed as NIDDM and treated with oral hypoglycemic agents. It has been speculated that these patients have a retarded form of IDDM. It is possible that the combination of specific Class II antigen molecule(s) and an invading antigen (virus, bacterium, chemical etc.) presented to the immune system triggers the formation of effector cells such as B lymphocytes and cytotoxic T lymphocytes which also cross-react with the pancreatic B cells. Multiple exposures to this or related antigens throughout several years may eventually lead a sufficient loss of pancreatic B cells to cause insulin dependence.</p>}}, author = {{Lernmark, A. and Baekkeskov, S. and Gerling, I. and Kastern, W. and Knutson, C. and Michelsen, B.}}, booktitle = {{Comparison of Type I and Type II Diabetes : Similarities and Dissimilarities in Etiology, Pathogenesis, and Complications}}, editor = {{Vranic, Mladen and Hollenberg, Charles H and Steiner, George}}, isbn = {{978-1-4757-1852-2}}, issn = {{0065-2598}}, language = {{eng}}, month = {{01}}, pages = {{107--127}}, series = {{Advances in Experimental Medicine and Biology}}, title = {{Immunological aspects of type 1 and 2 diabetes mellitus.}}, url = {{http://dx.doi.org/10.1007/978-1-4757-1850-8_7}}, doi = {{10.1007/978-1-4757-1850-8_7}}, volume = {{189}}, year = {{1985}}, }